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Metropolitan Sport Science Centre, University of Cape Town Medical School, South Africa.

1. The development of post-exercise ketosis is not abolished by the ingestion of glucose immediately after exercise, despite inducing high insulin/glucagon ratios in the peripheral (and therefore by implication in the portal) blood. 2. To investigate the possibility of autonomic control of the liver influencing its sensitivity to the major counter-regulatory hormones, we administered 50 g glucose, either on its own, or together with 0.5 mg prazosine, 40 mg propranolol, or 15 mg propantheline, to forty-seven 48 h carbohydrate-starved athletes who had just run 25 km. 3. The blood 3-hydroxybutyrate concentration rose from 0.30 +/- 0.05 (mean +/- S.E. of mean) to 0.52 +/- 0.08 mmol/l with exercise, and then to 1.32 +/- 0.40 mmol/l at 6 h after exercise in subjects who had ingested only glucose after exercise. 4. The effects of prazosine and propantheline on the blood ketone body concentration at 2 h after exercise was not statistically significant. Propranolol, on the other hand, significantly lowered the blood 3-hydroxybutyrate concentration (compared with controls) to 0.09 +/- 0.03 mmol/l at 3 h (P less than 0.01), and 0.35 +/- 0.08 mmol/l at 6 h (P less than 0.01) after exercise. 5. The plasma insulin, glucagon, glucose and free fatty acid concentrations were unaffected by propranolol, indicating that the antiketogenesis was the result of a direct effect on ketone body metabolism. 6. Since beta-adrenergic blockade has not previously been shown to have antiketogenic activity, except in somatostatin-induced hyperketonaemia, it is concluded that its effectiveness in post-exercise ketosis can probably be ascribed to a functional hepatic insulin and glucagon deficiency.